ArticleArthritis research & therapy2021
Mitochondrial protein CMPK2 regulates IFN alpha-enhanced foam cell formation, potentially contributing to premature atherosclerosis in SLE.
Article in Arthritis research & therapy, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers, 1 of them a synthesis that pooled it.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
24 citing papers in PubMed, 1 synthesis or guideline pooled it, 41 citations in OpenAlex.
- Macrophage-associated kinase signaling in atherosclerosis - a systematic review.Cell communication and signaling : CCS · 2026Pooled it
- The Multi-Omics Landscape of Enzymatic Alterations in Systemic Lupus Erythematosus.Proteomics. Clinical applications · 2026Article
- CMPK2 restrictsbioRxiv : the preprint server for biology · 2026Article
- MSC-derived exosomes ameliorate systemic lupus erythematosus by reprogramming macrophage mitochondrial homeostasis via the CMPK2-cGAS-STING axis.Journal of nanobiotechnology · 2026Article
- Ferroptosis: key regulatory pathways and their implications in cardiovascular pathophysiology.Frontiers in cardiovascular medicine · 2026Review
- Biological functions and clinical implications of the CMPK2 across multisystemic diseases.Cell & bioscience · 2025Review
- Targeted drug delivery systems for atherosclerosis.Journal of nanobiotechnology · 2025Review
- Induction of LY6E regulates interleukin-1β production, potentially contributing to the immunopathogenesis of systemic lupus erythematosus.Cell communication and signaling : CCS · 2025Article
- Macrophages Unmasked: Their Pivotal Role in Driving Atherosclerosis in Systemic Lupus Erythematosus.Clinical reviews in allergy & immunology · 2025Review
- Comprehensive Pan-cancer Analysis of CMPK2 as Biomarker and Prognostic Indicator for Immunotherapy.Current cancer drug targets · 2025Article
- Identification of NET formation and the renoprotective effect of degraded NETs in lupus nephritis.American journal of physiology. Renal physiology · 2024Article
- Multi-omics analysis uncovered systemic lupus erythematosus and COVID-19 crosstalk.Molecular medicine (Cambridge, Mass.) · 2024Article
- Transcriptomic Analysis of Cardiac Tissues in a Rodent Model of Coronary Microembolization.Journal of inflammation research · 2024Article
- Mitochondrial-related hub genes in dermatomyositis: muscle and skin datasets-based identification andFrontiers in genetics · 2024Article
- Type I Interferons in Autoimmunity: Implications in Clinical Phenotypes and Treatment Response.The Journal of rheumatology · 2023Review
- Single-tailed heterocyclic carboxamide lipids for macrophage immune-modulation.Biomaterials science · 2023Article
- Low-Dose Radiation Affects Cardiovascular Disease Risk in Human Aortic Endothelial Cells by Altering Gene Expression under Normal and Diabetic Conditions.International journal of molecular sciences · 2022Article
- Identification of candidate biomarkers and pathways associated with type 1 diabetes mellitus using bioinformatics analysis.Scientific reports · 2022Article
- Immune-Related Protein Interaction Network in Severe COVID-19 Patients toward the Identification of Key Proteins and Drug Repurposing.Biomolecules · 2022Article
- The mitochondrial gene-CMPK2 functions as a rheostat for macrophage homeostasis.Frontiers in immunology · 2022Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundPremature atherosclerosis occurs in patients with SLE; however, the mechanisms remain unclear. Both mitochondrial machinery and proinflammatory cytokine interferon alpha (IFN-α) potentially contribute to atherogenic processes in SLE. Here, we explore the roles of the mitochondrial protein cytidine/uridine monophosphate kinase 2 (CMPK2) in IFN-α-mediated pro-atherogenic events.
methodsFoam cell measurements were performed by oil red O staining, Dil-oxLDL uptake and the BODIPY approach. The mRNA and protein levels were measured by qPCR and Western blotting, respectively. Isolation of CD4+ T cells and monocytes was performed with monoclonal antibodies conjugated with microbeads. Manipulation of protein expression was conducted by either small interference RNA (siRNA) knockdown or CRISPR/Cas9 knockout. The expression of mitochondrial reactive oxygen species (mtROS) was determined by flow cytometry and confocal microscopy.
resultsIFN-α enhanced oxLDL-induced foam cell formation and Dil-oxLDL uptake by macrophages. In addition to IFN-α, several triggers of atherosclerosis, including thrombin and IFN-γ, can induce CMPK2 expression, which was elevated in CD4+ T cells and CD14+ monocytes isolated from SLE patients compared to those isolated from controls. The analysis of cellular subfractions revealed that CMPK2 was present in both mitochondrial and cytosolic fractions. IFN-α-induced CMPK2 expression was inhibited by Janus kinase (JAK)1/2 and tyrosine kinase 2 (Tyk2) inhibitors. Both the knockdown and knockout of CMPK2 attenuated IFN-α-mediated foam cell formation, which involved the reduction of scavenger receptor class A (SR-A) expression. CMPK2 also regulated IFN-α-enhanced mtROS production and inflammasome activation.
conclusionsThe study suggests that CMPK2 plays contributing roles in the pro-atherogenic effects of IFN-α.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.